Our studies have demonstrated that alcohol abuse leads to a decrease in the level of long chain polyunsaturated fatty acids like arachidonate (20:4n6) and docosahexaenoate (22:6n3). It is hypothesized that the lowered level of these important cell membrane constituents leads to alterations in cellular function that may underlie some aspects of alcohol-induced organ injuries and that prevention or restoration of this decrement in essential fatty acids may be of therapeutic benefit to alcoholics. Recent studies have focused upon elucidating the ability of humans to biosynthesize these fatty acids in vivo from their 18-carbon precursors in order to gain a better understanding of the ability of humans to compensate for their losses, for example, in the liver. It has been demonstrated for the first time that humans can biosynthesize 20:4n6 in vivo and that this capability is developed at least by 33 weeks gestational age in infants. The largest controlled dietary studies thus far conducted have shown that increased levels of long chain n-3 fatty acids like 20:5n3 and 22:6n3 in the diet lead to a lower accretion of n-3 metabolites in vivo. Progress has also been made in developing a rat model of extreme neural 22:6n3 deficiency using the artificial rearing where the diet may be controlled throughout nearly the entire life cycle. Behavioral studies indicate poorer performance on social learning tasks in rats with lower levels of brain 22:6n3.